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ME/CFS B-Cell Study/Rituximab Implications

Discussion in 'Latest ME/CFS Research' started by Gemini, Dec 7, 2012.

  1. Gemini

    Gemini Senior Member

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    August59, Enid, Ema and 2 others like this.
  2. snowathlete

    snowathlete

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    Interesting though I cant think what this means in the overall picture.
  3. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    Perhaps looking at other protocols as well as Ritubimab that work on B cells? Viruses such as EBV seem to infect B cells.

    Sushi
  4. Valentijn

    Valentijn Activity Level: 3

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    So they're using a real ME definition - great to see that happening in the UK! Also nice to see the Rituximab research sparking interest from immunology researchers who weren't previously active in the ME arena.

    Also very interesting stuff. I think they're basically saying that we have a normal amount of B cells, just too many naive (unexposed to antigen) and transitional B cells (exposed to an antigen but not released from lymph nodes?), which would seem to imply that we have a low amount of circulating mature B cells. I think :p

    It looks like the plasmablasts are created from (mature?) B cells, so those might be low as a result of insufficient numbers of mature B cells.

    I'm a little confused by their conclusion regarding "a subtle tendency to autoimmunity", since they also state:
    (Their typo, not mine. For a change.)

    Should be interesting to read the entire thing, if someone has access.
  5. alex3619

    alex3619 Senior Member

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    The WPI said something similar years ago. Due to all the XMRV controversy this got ignored. Its a step in the right direction, we need more research into these issues.
    taniaaust1 likes this.
  6. snowathlete

    snowathlete

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    That typo could be 'not' but it could be something else. It seems an odd statement to me if it is 'not' because arguably we do have symptoms of autoimmunity, and as already pointed out, this seems to conflict with their subsequent statement.

    Anyway would these higher types of b cells mean that we had lower than normal levels of antibody producing B cells? But I'd have though Rituximab makes that situation worse, at least at first. As there seems to be a delay after Rituximab before patients improve, perhaps that corrects the levels meaning we get more antibodies but is be surprised if it was that simple and direct.

    So much we don't know.
  7. snowathlete

    snowathlete

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    Does anyone know how these results compare to known autoimmune diseases?

    The statement, "a subtle tendency to autoimmunity", might suggest that they have seen the same sort of B cell type proportions elsewhere.
  8. taniaaust1

    taniaaust1 Senior Member

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    Ive had symptoms of autoimmunity.. my frozen shoulder when I was in my 30s, specialist said it must of been caused by that due to the age when my issue happened and hence why I had an abnormal state of healing happen. Ive heard of many of us having some kind of issues. (he put it down to my insulin issue as he couldnt think of anything else but surely I wouldnt be getting diabetes complications before Im even a diabetic with only a prediabetes state).

    Maybe the ones who wrote that didnt know that many of us do at times get signs of autoimmunity.
    ...............

    This new study is exciting and Im so happy they used the Canadian definition as well so we all at least know it was a good patient group which was used. (I hope they get a lot of thank yous from the ME/CFS community esp since we have such a reputation of knocking studies thou of cause they are usually poorly done ones who get our knocking).

    Wondering if Dr Wessely or one of his boys will be involved now in doing a study on this same thing with his CFS criteria. He wont be happy about this study. (maybe he's got a new psych study ready for others to publish for him if this new study starts looking like it may make too much news). Study like this is damaging on his views.
  9. taniaaust1

    taniaaust1 Senior Member

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    This study should be used to push Advocacy efforts into more government funding as we need to get these studies done (using the same canadian criteria). It should be a priority.

    We should make sure our societies are pushing for more funding and using this study as an example of one of the areas of study need.
  10. Marco

    Marco Old blackguard

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    'Patients with CFS do no(t) have .......symptoms of autoimmunity'

    I'd like to see the full paper to read this in context but this strikes me as a strange conclusion.

    I would have thought that the symptoms would reflect the organ affected in single organ disorders or; if systemic, there would be a wide range of symptoms that would largely overlap with ME/CFS symptomology.

    Are there symptoms that are common in autoimmune diseases but not in other types of disease?

    I can't find a reliable source of 'common autoimmune symptoms'.

    This summary is the best I can find at the moment :

    http://www.allergy.org.au/patients/autoimmunity/autoimmune-diseases
    Valentijn likes this.
  11. grosolo

    grosolo

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    the neuroinflammation up my spine and into my head, the lesions on my brain -- those are very clearly signs of autoimmunity, the way my body is always wired and i don't get colds, and when i finally do get colds i actually sleep -- all very much signs of autoimmunity. i'm happy about this paper but we all know that where we are in the me research right now is way ahead of where these scientists are: namely, we all know here already that there are definitely subsets of patients. some might be totally in the autoimmune camp (I know I'm one) and others may not, and the people studied for this probably are not. And that's fine. But it's very dangerous for us to have researchers like these saying what ME definitely is or isn't when a) they're not right, not across the board and b) ME 100 percent isn't one thing. And if the public believes it is, then every time some new paper saying this is exactly what ME is comes out, we're going to be at the mercy of the public's reaction to that one paper. that's why the XMRV fiasco was both so compelling and then so very defeating. we can't repeat that. the public needs to understand the multifariousness of this disease so that we're not doomed to repeat their sudden interest and then disinterest, so that people stop speaking for us who don't have the authority to...

    I really hope people on here feel the way I do about this...i'm so tired of every one jumping on one thing, like this is gonna be the thing. i mean, i know for me, i'm looking toward the autoimmunity stuff, toward b cells, toward rituximab, yes. but i know my reality, while very complicated, is just my reality. and while others may share it, they may only share parts but not the entire whole and that still others may be very different...
    jeffrez, Little Bluestem, Lou and 3 others like this.
  12. Legolas

    Legolas

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  13. Valentijn

    Valentijn Activity Level: 3

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    So it looks like they got interested in a similar way that the Rituximab researchers did.

    So it might be more involved than simply depleting B-cells, though that seems to be an important aspect.


    I think they're suggesting that autoimmunity may be a milder result on a spectrum that also includes immune deficiency.

    I think this is what they're trying to figure out in this study, or at least getting a better idea about.

    They also talk about auto-reactive B-cells usually getting destroyed when they're made, and speculate that we might have a problem with that destructive process.

    ZOMG, we're being compared to people wot have real diseases! :cool:

    At some point, B cells can become either follicular B-cells or marginal zone B-cells. Follicular B-cells might become plasmablasts or memory B-cells, but the marginal zone B-cells always become plasmablasts.

    They also seem very interested in eventually studying the B-cells before and after Rituximab use, to see how that alters B-cell populations. They're also interested in whether severe patients have more extreme results, since they were just studying moderate cases where some immune symptoms were only intermittent.


    I don't much like the statement of possibility that B cells are the result, not the cause (which could imply our B-cells are messed up as a result of a theoretical false illness belief causing inactivity). But I think it's a good thing that they're admitting the issue isn't settled, instead of taking a political stance. Much more respectable than the conclusions psychological researchers to draw out of thin air anyhow :p
  14. Valentijn

    Valentijn Activity Level: 3

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    Also:
    If anyone's wondering where to make donations :p
  15. user9876

    user9876 Senior Member

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  16. Jenny

    Jenny Senior Member

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    Does anyone in the UK see Dr Bansal?
  17. Marco

    Marco Old blackguard

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    I'm beginning to think its a pity they were excluded.

    If included and analysed separately we might have learned something. They may have had the same profile as controls; the same as the rest of the 'CFS' cohort; an altered profile in the opposite direction or perhaps even a more extreme profile than the rest of the cohort.
  18. liquid sky

    liquid sky Senior Member

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    Interesting study. Thanks for posting
  19. Enid

    Enid Senior Member

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    Thanks Gemini for posting - very interesting findings - as they say all grist to the mill (of understanding ME). Another move forward.
    justy likes this.
  20. Gemini

    Gemini Senior Member

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    I agree completely.

    Advocates should make the FDA aware of this study's conclusion that "The therapeutic response to Rituximab suggests B-cells are somehow involved in the pathogenesis or perpetuation of CFS symptoms."

    janet.woodcock@fda.hhs.gov Dir. Center of Drug Evaluation & Research
    sandra.kweder@fda.hhs.gov Deputy Dir. of the Office of New Drugs

    Researchers planning ME/CFS Rituximab trials should consider Dr. Bansal's interest "to monitor B-cell subsets of CFS patients before and after Rituximab treatment and monitor repopulation of the different B-cell subsets with the return of symptoms."

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